urate, and urea) was examined in 7364 middle aged British men. After allowing for the influence of alcohol consumption on serum biochemistry there was no substantial association of increased blood lead concentration with renal function. There was a weak positive trend towards increased serum urate concentration at high blood lead concentration and a reverse trend for serum urea concentration. These findings differ from those of a previous study carried Cardiac arrhythmias during rewarming of patients with accidental hypothermia ANDREW C RANKIN, ALAN P RAE Abstract Accidental hypothermia has a high mortality and is associated with cardiac arrhythmias. To determine the incidence of arrhythmias and their importance 22 patients with accidental hypothermia (core temperature <35°C) were studied by 12 lead electrocardiography and continuous recording of cardiac rhythm. Although 14 of the patients died (64%), only six died while hypothermic. Prolongation of theQ-T interval and the presence of J waves were related to the severity of the hypothermia. Supraventricular arrhythmias, including atrial fibrillation, were common (nine cases) and benign.

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Adenosine may be of therapeutic and diagnostic value in the emergency management of arrhythmias. It causes transient atrioventricular nodal block and thus ends paroxysmal supraventricular tachycardias that involve the atrioventricular node. Also, it may uncover underlying atrial arrhythmias by slowing the ventricular response. Its duration of action is brief and serious adverse effects have not been reported. A 12 year old patient with atrial flutter is presented, in whom intravenous adenosine was followed by acceleration of the heart rate to a potentially dangerous arrhythmia. (Br Heart J 1993;69:263-265) Adenosine is an endogenous purine nucleoside that causes atrioventricular nodal block when injected intravenously.' 2 It is effective, therefore, to end paroxysmal supraventricular tachycardias that have a re-entrant circuit that includes the atrioventricular node.Y4 With atrial arrhythmias, such as atrial flutter, adenosine induced atrioventricular nodal block may be of diagnostic value by slowing the ventricular response to show the underlying atrial tachyarrhythmia.3-5 Transient side effects, including chest discomfort, flushing, and dyspnoea, are common, but serious adverse effects of adenosine have not been reported. This may be attributable to its extreme brevity of action because of rapid metabolism and removal from blood.7 We report a case where intravenous administration of adenosine was followed by an increase in the ventricular response to atrial flutter, with a resultant potentially life threatening arrhythmia. Case report A 12 year old boy was admitted to hospital after an episode of syncope. He had a history of Mustard repair of transposition of the great arteries at the age of 10 months. After the repair of an atrial baffle leak one year before the present admission, he had undergone implantation of a permanent ventricular pacemaker (Medtronic "Activitrax II", VVI-R) for symptomatic sinus node dysfunction. He had continued to complain of episodes of dizziness, the aetiology of which was not identified.On admission he was well with no evidence of heart failure. Heart rate was 120 beats/min and he was normotensive, with a blood pressure of 109/58 mm Hg. An electrocardiogram showed a narrow complex tachycardia. To clarify the diagnosis of the tachycardia, and possibly restore normal rhythm, adenosine was given intravenously with incremental boluses of 0 1, 02, and 0-4 mg/kg (4, 8, and 16 mg). Transient symptoms of increasing severity (flushing, non-specific malaise) were reported with each dose. After the 8 mg dose of adenosine, the ventricular rate briefly slowed to 86 beats/min (for four seconds) but then increased to 235 beats/min. This rapid rate persisted for three minutes before settling to 120 beats/min. A further dose (16 mg) was given. This slowed the ventricular rate so that the pacemaker paced the ventricle at 60 beats/min for 10 seconds ( fig IA). During this period of ventricular slowing, underlying atrial flutter waves at 280 beats/min were apparent. The ventricular respons...

morphologically and with the help of immunocytochemistry. There was no staining by antibodies CK 1 (Dako) or CAM 5.2 (Becton-Dickinson) to intracellular cytokeratin antigens. All the tumours stained positively for vimentin but not for desmin or leucocyte common antigen. The main differential diagnosis of spindle cell squamous carcinoma was excluded in each case.

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